ArticleCell reports2018
Mild Impairment of Mitochondrial OXPHOS Promotes Fatty Acid Utilization in POMC Neurons and Improves Glucose Homeostasis in Obesity.
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Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
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- Neuron-periphery mitochondrial stress communication in aging and diseases.Life medicine · 2022Review
- Food craving-like episodes during pregnancy are mediated by accumbal dopaminergic circuits.Nature metabolism · 2022Article
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- Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation.Cell & bioscience · 2022Article
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- TLR4-interactor with leucine-rich repeats (TRIL) is involved in diet-induced hypothalamic inflammation.Scientific reports · 2021Article
- Central Acting Hsp10 Regulates Mitochondrial Function, Fatty Acid Metabolism, and Insulin Sensitivity in the Hypothalamus.Antioxidants (Basel, Switzerland) · 2021Article
- Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan.Antioxidants (Basel, Switzerland) · 2021Review
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- Systemic effects of mitochondrial stress.EMBO reports · 2020Review
- GLP-1 Receptor Signaling in Astrocytes Regulates Fatty Acid Oxidation, Mitochondrial Integrity, and Function.Cell metabolism · 2020Article
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- Two human patient mitochondrial pyruvate carrier mutations reveal distinct molecular mechanisms of dysfunction.JCI insight · 2019Article
- The melanocortin pathway and control of appetite-progress and therapeutic implications.The Journal of endocrinology · 2019Review
- Hypothalamic Fatty Acids and Ketone Bodies Sensing and Role of FAT/CD36 in the Regulation of Food Intake.Frontiers in physiology · 2019Review
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Authors and funding
16 authors at 8 institutions in 4 countries.
Katharina TimperMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Lars PaegerExcellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Biocenter, University of Cologne, Cologne, Germany.
Carmen Sánchez-LasherasMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Luis VarelaDepartment of Biochemistry and Fraternal Order of Eagles Diabetes Research Center, Caver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Alexander JaisMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Hendrik NolteExcellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Merly C VogtMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
A Christine HausenMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Christian HeilingerMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Nadine EversMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
J Andrew PospisilikMax-Planck-Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany.
Josef M PenningerIMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr Gasse 3, 1030 Vienna, Austria.
Eric B TaylorDepartment of Biochemistry and Fraternal Order of Eagles Diabetes Research Center, Caver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Tamas L HorvathMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Program in Integrative Cell Signaling and Neurobiology of Metabolism, Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Anatomy and Histology, University of Veterinary Medicine, Budapest, Hungary.
Peter KloppenburgExcellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Biocenter, University of Cologne, Cologne, Germany.
Jens Claus BrüningMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany. Electronic address: bruening@sf.mpg.de.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity Hospital Cologne · DEMax Planck Institute for Metabolism Research · DEUniversity of Cologne · DEUniversity of Iowa · USAustrian Academy of Sciences · ATMax Planck Institute of Immunobiology and Epigenetics · DEYale University · US
Funding
Regulation of Hepatic Macronutrient Metabolism by Mitochondrial Citrate TransportR01DK104998 · NIDDK · UNIVERSITY OF IOWA · PI TAYLOR, ERIC B · 2015 to 2022
$3.2MFeeding Driven by POMC NeuronsR01DK111178 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2017 to 2020
$1.9MNIDDK NIH HHS R01 DK104998NIDDK NIH HHS R01 DK111178
Abstract
Mitochondrial oxidative phosphorylation (OXPHOS) and substrate utilization critically regulate the function of hypothalamic proopiomelanocortin (POMC)-expressing neurons. Here, we demonstrate that inactivation of apoptosis-inducing factor (AIF) in POMC neurons mildly impairs mitochondrial respiration and decreases firing of POMC neurons in lean mice. In contrast, under diet-induced obese conditions, POMC-Cre-specific inactivation of AIF prevents obesity-induced silencing of POMC neurons, translating into improved glucose metabolism, improved leptin, and insulin sensitivity, as well as increased energy expenditure in AIF
Indexed as
HomeostasisOxidative PhosphorylationAnimalsApoptosis Inducing FactorDiet, High-FatEnergy MetabolismFatty AcidsGlucoseGlucose IntoleranceHypothalamusMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseMitochondriaAIFM1 protein, mouseApoptosis Inducing FactorFatty AcidsGlucosePro-OpiomelanocortinAIFapoptosis-inducing factorfatty acidhypothalamic POMC-neuronsmitochondrialmitochondrial oxidative phosphorylationMPC-1obesityoxidationpyruvate carrier-1reactive oxygen speciesROS
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